JNM: FDG PET shows aortic inflammation in COPD patients
Patients with chronic obstructive pulmonary disease (COPD) exhibit increased aortic inflammation, even after controlling for smoking. FDG PET might be useful to test the anti-inflammatory effect of future drug therapies in COPD and allow mechanistic evaluation of the increased cardiovascular risk to be explored, according to a study in this month's Journal of Nuclear Medicine.
Patients with COPD would have more arterial inflammation than controls. To test this hypothesis, James M. Coulson, MBBCh, clinical lecturer at Wales Heart Research Institute and School of Medicine at Cardiff University in Cardiff, England, and colleagues measured arterial inflammation in male ex-smokers with COPD and in male ex-smokers without COPD (negative controls) using FDG PET/CT.
Coulson and colleagues also enrolled men with two or more components of the metabolic syndrome (International Diabetes Federation criteria) to act as positive controls for the study, since metabolic syndrome is associated with excessive cardiovascular risk and is known to cause increased arterial inflammation on FDG PET.
The researchers expressed aortic inflammation as the target-to-background ratio of the standardized uptake value in seven male ex-smokers with COPD, seven male ex-smokers free from COPD and five men with metabolic syndrome.
Abdominal aortic mean target-to-background ratio was greater in COPD patients than in ex-smoker controls (1.60 vs. 1.34). Aortic arch and abdominal aorta mean TBRs were higher in metabolic syndrome patients than in COPD patients (aortic arch, 1.80 vs. 1.53 and abdominal aorta, 1.71 vs. 1.60), according to Coulson and colleagues.
“COPD patients exhibited aortic inflammation that fell between the aortic inflammation exhibited by ex-smokers and that by metabolic syndrome patients. This may in part explain the increased risk of cardiovascular disease in COPD patients,” concluded Coulson and colleagues.
Although the number of subjects studied was small, the study showed significant differences among the groups in terms of aortic inflammation, wrote Coulson and colleagues.
Future larger studies, well matched for smoking history, are needed to determine the clinical relevance of these findings in terms of the prediction of cardiovascular events in this high-risk patient group, added the authors.
Patients with COPD would have more arterial inflammation than controls. To test this hypothesis, James M. Coulson, MBBCh, clinical lecturer at Wales Heart Research Institute and School of Medicine at Cardiff University in Cardiff, England, and colleagues measured arterial inflammation in male ex-smokers with COPD and in male ex-smokers without COPD (negative controls) using FDG PET/CT.
Coulson and colleagues also enrolled men with two or more components of the metabolic syndrome (International Diabetes Federation criteria) to act as positive controls for the study, since metabolic syndrome is associated with excessive cardiovascular risk and is known to cause increased arterial inflammation on FDG PET.
The researchers expressed aortic inflammation as the target-to-background ratio of the standardized uptake value in seven male ex-smokers with COPD, seven male ex-smokers free from COPD and five men with metabolic syndrome.
Abdominal aortic mean target-to-background ratio was greater in COPD patients than in ex-smoker controls (1.60 vs. 1.34). Aortic arch and abdominal aorta mean TBRs were higher in metabolic syndrome patients than in COPD patients (aortic arch, 1.80 vs. 1.53 and abdominal aorta, 1.71 vs. 1.60), according to Coulson and colleagues.
“COPD patients exhibited aortic inflammation that fell between the aortic inflammation exhibited by ex-smokers and that by metabolic syndrome patients. This may in part explain the increased risk of cardiovascular disease in COPD patients,” concluded Coulson and colleagues.
Although the number of subjects studied was small, the study showed significant differences among the groups in terms of aortic inflammation, wrote Coulson and colleagues.
Future larger studies, well matched for smoking history, are needed to determine the clinical relevance of these findings in terms of the prediction of cardiovascular events in this high-risk patient group, added the authors.